Metabolic acidosis & Metabolic alkalosis Dr.R.Anitha Prof.S.Shivakumar unit

Metabolic acidosis

Primary Change Secondary change Net effect  Hco3  Pco2  pH ( H+) Pco2 should  by 1.2 mmHg for each mEq  plasma Hco3

Causes of metabolic acidosis Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea

Normal anion gap or hyper chloremic acidosis AG = Na+– (Hco3  + Cl ) Normal = 12 ± 4 ( 8  16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap

Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis

Clinical features Kussmals respiration (increased depth than rate) Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia

Treatment Treat the underlying cause NaHCO3 therapy: Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning

NaHCO3 therapy in severe acidosis: pH <7.1 Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 – observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and 18 meq/L in NAG

Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH 7.0 HCO3 5 pCo2 20.8 Urine ketones + BP 100/70 PR 128/min Start IV saline 0.9%, insulin bolus &continuous infusion drip, start NaHCO3 therapy to bring the pH to 7.2

Calculation of desired HCO3 H = 24 x Pco2 (Modified Henderson equation) Hco3 pH = 7.0 HC03 = 5 PCo2 =20.8 When pH is 7.0, H+ = 100 neq To make the pH 7.2, H+ = 63, the desired HCO3(y) 63 = 24 x 20.8/ y y = 24 x 20.8/ 63 = 7.9 = desired HCO3 NaHCO3 dose= desired HCO3 – observed HCO3 * 50%of body wt = 7.9 – 5 * 25 = 73 meq

Complications of NaHCO3 therapy Sodium and volume overload – dangerous in states of shock – slow continuous UF/ CVVH/intermittent dialysis(HD/PD) Hypernatremia Hypokalemia Overshoot alkalosis On correction of the cause metabolism of organic anions(lactate, ketoacids) will produce HCO3 – potential HCO3

CHRONIC ACIDOSIS Imeq/kg/day of alkali either as Shohl’s solution or NaHCO3 tablets Shohl’s solution = 140g citric acid + 98g hydrated crystalline salt of sodium citrate in dist water to make 1000ml ( 1ml=1meq)

Potassium in metabolic acidosis Usually hyperkalemia occurs Potassium depletion common – GI loss/renal loss/treatment of DKA Initial plasma K relatively normal or high – metabolic acidemia cause K to move out of cells in to ECF. Careful freq monitoring of potassium during treatment and correct hypokalemia (<3.5) at once.

Summary AG Normal Anion Gap High Anion Gap cause H/O diarrhoea,DM, Toxin ingestion, C/F of shock Sr Ketone, lactate, urine pH/osm gap/AG, pl osm gap Treat The cause The pH only in severe acidosis pH<7.1

Metabolic alkalosis

Pco2 should  by 0.6 mmHg for each mEq  plasma Hco3 Primary Change Secondary change Net effect  Hco3  Pco2  pH ( H+) Pco2 should  by 0.6 mmHg for each mEq  plasma Hco3

Metabolic alkalosis Generation Maintenance H+ loss in GIT (vomiting or NG suction) or in urine (diuretics) Maintenance Perpetuation of metabolic alkalosis – requires impairment in renal HCO3 excretion

Maintenance Decreased effective arterial volume Decreased GFR Secondary hyperaldosteronism Na retention/H+ excretion

Chloride depletion Chloride loss reabsorption Bicarbonate Increase

Potassium depletion Intracellular acidosis Paradoxical aciduria k k k H k H H H H k k k k H H k k k H H H k H k H Paradoxical aciduria Extracellular alkalosis

Cause of metabolic alkalosis Gastrointestinal loss vomiting or NG suction Renal loss Loop or thiazide diuretic Mineralocorticoid excess Postchronic hypercapnea H+ movement into cells Hypokalemia

For a clinically relevant etiologic classification Urine Cl- conc <10meq/L Chloride Depletion Alkalosis Decreased effective arterial volume CDA >20meq/L Potassium Depletion Alkalosis Mineralocorticoid excess KDA

CDA KDA Gastric acid loss Chloruretic diuretics Posthypercapnic state With hypertension Primary aldosteronism Secondary aldosteronism With normotension Bartter syndrome Gitelman syndrome

Clinical features Signs of volume depletion in CDA (hypotension, tachycardia..) Singn of volume expansion in KDA (hypertension) Signs of hypokalemia In severe metabolic alkalosis (pH > 7.55) hepatic encephalopathy, cardiac arrhythmia, digitalis cardiotoxicty or altered mental status

General management principles Correction of fluid defecit Correction of hypokalemia and hypochloremia Correction of pH if it is severe alkalosis (pH > 7.55)

Chloride Depletion Alkalosis ECF volume contraction Volume correction by NaCl Further repletion KCl ECF volume overload NaCl contraindicated T.Acetazolamide 250mg bd/tds

Potassium depletion alkalosis Potassium replacement Removal of source of mineralocorticoid excess Blockade – Amiloride 5-10mg Triamtrene 100 mg bd Spiranalactone 25-100 mg Hypomagnesemia to be corrected

Severe hypokalemia (<2meq/l) Make the metabolic alkalosis and hypovolemia resistant to saline therapy Because severe hypokalemia cause impairment in Cl- reabsorption in distal tubule Replacement of only one half of potassium defecit will normalise Cl- reabsorption

In very severe alkalosis (pH > 7.55) c/f of hepatic encephalopathy, cardiac arrhythmia, digitalis cardiotoxicty or altered mental status HCl (0.1N)administration in central venous catheter 25meq/hr Amount of HCl= 0.5* body wt*(plasma HCO3-24)

Summary Urine cl Chloride depletion alkalosis (CDA) Potassium depletion alkalosis (KDA) CDA ECF vol contraction – NaCl, KCl ECF vol overload – acetazolamide, K supp KDA K replacement Remove or block the source

Summary cont… pH >7.55 Hcl therapy

Take home message Identify the cause with history, C/F, ABG, lab analysis. Single HCO3 value cannot replace ABG Treat the cause Treat the pH only when there is severe acidosis or alkalosis Always correct the pH not the HCO3

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